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Fusion gene ID: 28739 |
FusionGeneSummary for PRKCD_PRKCD |
 Fusion gene summary |
| Fusion gene information | Fusion gene name: PRKCD_PRKCD | Fusion gene ID: 28739 | Hgene | Tgene | Gene symbol | PRKCD | PRKCD | Gene ID | 5580 | 5580 |
| Gene name | protein kinase C delta | protein kinase C delta | |
| Synonyms | ALPS3|CVID9|MAY1|PKCD|nPKC-delta | ALPS3|CVID9|MAY1|PKCD|nPKC-delta | |
| Cytomap | 3p21.1 | 3p21.1 | |
| Type of gene | protein-coding | protein-coding | |
| Description | protein kinase C delta typeprotein kinase C delta VIIItyrosine-protein kinase PRKCD | protein kinase C delta typeprotein kinase C delta VIIItyrosine-protein kinase PRKCD | |
| Modification date | 20180523 | 20180523 | |
| UniProtAcc | Q05655 | Q05655 | |
| Ensembl transtripts involved in fusion gene | ENST00000394729, ENST00000330452, ENST00000477794, | ENST00000394729, ENST00000330452, ENST00000477794, | |
| Fusion gene scores | * DoF score | 4 X 5 X 2=40 | 3 X 4 X 3=36 |
| # samples | 5 | 4 | |
| ** MAII score | log2(5/40*10)=0.321928094887362 effective Gene in Pan-Cancer Fusion Genes (eGinPCFGs). DoF>8 and MAII>0 | log2(4/36*10)=0.15200309344505 effective Gene in Pan-Cancer Fusion Genes (eGinPCFGs). DoF>8 and MAII>0 | |
| Context | PubMed: PRKCD [Title/Abstract] AND PRKCD [Title/Abstract] AND fusion [Title/Abstract] | ||
| Functional or gene categories assigned by FusionGDB annotation | |||
| * DoF score (Degree of Frequency) = # partners X # break points X # cancer types ** MAII score (Major Active Isofusion Index) = log2(# samples/DoF score*10) |
| Gene ontology of each fusion partner gene with evidence of Inferred from Direct Assay (IDA) from Entrez |
| Partner | Gene | GO ID | GO term | PubMed ID |
| Hgene | PRKCD | GO:0006468 | protein phosphorylation | 10713049|16611985 |
| Hgene | PRKCD | GO:0006915 | apoptotic process | 10770950 |
| Hgene | PRKCD | GO:0016572 | histone phosphorylation | 19059439 |
| Hgene | PRKCD | GO:0018105 | peptidyl-serine phosphorylation | 18285462 |
| Hgene | PRKCD | GO:0018107 | peptidyl-threonine phosphorylation | 10770950 |
| Hgene | PRKCD | GO:0032147 | activation of protein kinase activity | 10713049 |
| Hgene | PRKCD | GO:0042119 | neutrophil activation | 10770950 |
| Hgene | PRKCD | GO:0070301 | cellular response to hydrogen peroxide | 10713049 |
| Hgene | PRKCD | GO:0071447 | cellular response to hydroperoxide | 19059439 |
| Hgene | PRKCD | GO:1904385 | cellular response to angiotensin | 18285462 |
| Tgene | PRKCD | GO:0006468 | protein phosphorylation | 10713049|16611985 |
| Tgene | PRKCD | GO:0006915 | apoptotic process | 10770950 |
| Tgene | PRKCD | GO:0016572 | histone phosphorylation | 19059439 |
| Tgene | PRKCD | GO:0018105 | peptidyl-serine phosphorylation | 18285462 |
| Tgene | PRKCD | GO:0018107 | peptidyl-threonine phosphorylation | 10770950 |
| Tgene | PRKCD | GO:0032147 | activation of protein kinase activity | 10713049 |
| Tgene | PRKCD | GO:0042119 | neutrophil activation | 10770950 |
| Tgene | PRKCD | GO:0070301 | cellular response to hydrogen peroxide | 10713049 |
| Tgene | PRKCD | GO:0071447 | cellular response to hydroperoxide | 19059439 |
| Tgene | PRKCD | GO:1904385 | cellular response to angiotensin | 18285462 |
| Fusion gene information from three resources (ChiTars (NAR, 2018), tumorfusions (NAR, 2018), Gao et al. (Cell, 2018)) * All genome coordinats were lifted-over on hg19. * Click on the break point to see the gene structure around the break point region using the UCSC Genome Browser. |
| Data type | Source | Cancer type | Sample | Hgene | Hchr | Hbp | Hstrand | Tgene | Tchr | Tbp | Tstrand |
| ChiTaRS3.1 | AI457515 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + | ||
| ChiTaRS3.1 | AK130023 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| * LD: Li Ding group's fusion gene list RV: Roel Verhaak group's fusion gene list ChiTaRs fusion database |
| Open reading frame (ORF) analsis of fusion genes based on Ensembl gene isoform structure. * Click on the break point to see the gene structure around the break point region using the UCSC Genome Browser. |
| ORF | Henst | Tenst | Hgene | Hchr | Hbp | Hstrand | Tgene | Tchr | Tbp | Tstrand |
| 3UTR-3CDS | ENST00000394729 | ENST00000394729 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| 3UTR-3CDS | ENST00000394729 | ENST00000330452 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| 3UTR-intron | ENST00000394729 | ENST00000477794 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| 3UTR-3CDS | ENST00000330452 | ENST00000394729 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| 3UTR-3CDS | ENST00000330452 | ENST00000330452 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| 3UTR-intron | ENST00000330452 | ENST00000477794 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| intron-3CDS | ENST00000477794 | ENST00000394729 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| intron-3CDS | ENST00000477794 | ENST00000330452 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| intron-intron | ENST00000477794 | ENST00000477794 | PRKCD | chr3 | 53226458 | - | PRKCD | chr3 | 53217182 | + |
| intron-3UTR | ENST00000394729 | ENST00000394729 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-3UTR | ENST00000394729 | ENST00000330452 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-intron | ENST00000394729 | ENST00000477794 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-3UTR | ENST00000330452 | ENST00000394729 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-3UTR | ENST00000330452 | ENST00000330452 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-intron | ENST00000330452 | ENST00000477794 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-3UTR | ENST00000477794 | ENST00000394729 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-3UTR | ENST00000477794 | ENST00000330452 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
| intron-intron | ENST00000477794 | ENST00000477794 | PRKCD | chr3 | 53226919 | + | PRKCD | chr3 | 53226391 | + |
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FusionProtFeatures for PRKCD_PRKCD |
| Main function of each fusion partner protein. (from UniProt) |
| Hgene | Tgene |
| PRKCD | PRKCD |
| Calcium-independent, phospholipid- and diacylglycerol(DAG)-dependent serine/threonine-protein kinase that playscontrasting roles in cell death and cell survival by functioningas a pro-apoptotic protein during DNA damage-induced apoptosis,but acting as an anti-apoptotic protein during cytokine receptor-initiated cell death, is involved in tumor suppression as well assurvival of several cancers, is required for oxygen radicalproduction by NADPH oxidase and acts as positive or negativeregulator in platelet functional responses. Negatively regulates Bcell proliferation and also has an important function in self-antigen induced B cell tolerance induction. Upon DNA damage,activates the promoter of the death-promoting transcription factorBCLAF1/Btf to trigger BCLAF1-mediated p53/TP53 gene transcriptionand apoptosis. In response to oxidative stress, interact with andactivate CHUK/IKKA in the nucleus, causing the phosphorylation ofp53/TP53. In the case of ER stress or DNA damage-inducedapoptosis, can form a complex with the tyrosine-protein kinaseABL1 which trigger apoptosis independently of p53/TP53. In cytosolcan trigger apoptosis by activating MAPK11 or MAPK14, inhibitingAKT1 and decreasing the level of X-linked inhibitor of apoptosisprotein (XIAP), whereas in nucleus induces apoptosis via theactivation of MAPK8 or MAPK9. Upon ionizing radiation treatment,is required for the activation of the apoptosis regulators BAX andBAK, which trigger the mitochondrial cell death pathway. Canphosphorylate MCL1 and target it for degradation which issufficient to trigger for BAX activation and apoptosis. Isrequired for the control of cell cycle progression both at G1/Sand G2/M phases. Mediates phorbol 12-myristate 13-acetate (PMA)-induced inhibition of cell cycle progression at G1/S phase by up-regulating the CDK inhibitor CDKN1A/p21 and inhibiting the cyclinCCNA2 promoter activity. In response to UV irradiation canphosphorylate CDK1, which is important for the G2/M DNA damagecheckpoint activation. Can protect glioma cells from the apoptosisinduced by TNFSF10/TRAIL, probably by inducing increasedphosphorylation and subsequent activation of AKT1. Is highlyexpressed in a number of cancer cells and promotes cell survivaland resistance against chemotherapeutic drugs by inducing cyclinD1 (CCND1) and hyperphosphorylation of RB1, and via several pro-survival pathways, including NF-kappa-B, AKT1 and MAPK1/3(ERK1/2). Can also act as tumor suppressor upon mitogenicstimulation with PMA or TPA. In N-formyl-methionyl-leucyl-phenylalanine (fMLP)-treated cells, is required for NCF1 (p47-phox) phosphorylation and activation of NADPH oxidase activity,and regulates TNF-elicited superoxide anion production inneutrophils, by direct phosphorylation and activation of NCF1 orindirectly through MAPK1/3 (ERK1/2) signaling pathways. May alsoplay a role in the regulation of NADPH oxidase activity ineosinophil after stimulation with IL5, leukotriene B4 or PMA. Incollagen-induced platelet aggregation, acts a negative regulatorof filopodia formation and actin polymerization by interactingwith and negatively regulating VASP phosphorylation. Downstream ofPAR1, PAR4 and CD36/GP4 receptors, regulates differentiallyplatelet dense granule secretion; acts as a positive regulator inPAR-mediated granule secretion, whereas it negatively regulatesCD36/GP4-mediated granule release. Phosphorylates MUC1 in the C-terminal and regulates the interaction between MUC1 and beta-catenin. The catalytic subunit phosphorylates 14-3-3 proteins(YWHAB, YWHAZ and YWHAH) in a sphingosine-dependent fashion (Bysimilarity). Phosphorylates ELAVL1 in response to angiotensin-2treatment (PubMed:18285462). {ECO:0000250,ECO:0000269|PubMed:11748588, ECO:0000269|PubMed:11877440,ECO:0000269|PubMed:15774464, ECO:0000269|PubMed:16940418,ECO:0000269|PubMed:18285462, ECO:0000269|PubMed:19587372,ECO:0000269|PubMed:19801500}. | Calcium-independent, phospholipid- and diacylglycerol(DAG)-dependent serine/threonine-protein kinase that playscontrasting roles in cell death and cell survival by functioningas a pro-apoptotic protein during DNA damage-induced apoptosis,but acting as an anti-apoptotic protein during cytokine receptor-initiated cell death, is involved in tumor suppression as well assurvival of several cancers, is required for oxygen radicalproduction by NADPH oxidase and acts as positive or negativeregulator in platelet functional responses. Negatively regulates Bcell proliferation and also has an important function in self-antigen induced B cell tolerance induction. Upon DNA damage,activates the promoter of the death-promoting transcription factorBCLAF1/Btf to trigger BCLAF1-mediated p53/TP53 gene transcriptionand apoptosis. In response to oxidative stress, interact with andactivate CHUK/IKKA in the nucleus, causing the phosphorylation ofp53/TP53. In the case of ER stress or DNA damage-inducedapoptosis, can form a complex with the tyrosine-protein kinaseABL1 which trigger apoptosis independently of p53/TP53. In cytosolcan trigger apoptosis by activating MAPK11 or MAPK14, inhibitingAKT1 and decreasing the level of X-linked inhibitor of apoptosisprotein (XIAP), whereas in nucleus induces apoptosis via theactivation of MAPK8 or MAPK9. Upon ionizing radiation treatment,is required for the activation of the apoptosis regulators BAX andBAK, which trigger the mitochondrial cell death pathway. Canphosphorylate MCL1 and target it for degradation which issufficient to trigger for BAX activation and apoptosis. Isrequired for the control of cell cycle progression both at G1/Sand G2/M phases. Mediates phorbol 12-myristate 13-acetate (PMA)-induced inhibition of cell cycle progression at G1/S phase by up-regulating the CDK inhibitor CDKN1A/p21 and inhibiting the cyclinCCNA2 promoter activity. In response to UV irradiation canphosphorylate CDK1, which is important for the G2/M DNA damagecheckpoint activation. Can protect glioma cells from the apoptosisinduced by TNFSF10/TRAIL, probably by inducing increasedphosphorylation and subsequent activation of AKT1. Is highlyexpressed in a number of cancer cells and promotes cell survivaland resistance against chemotherapeutic drugs by inducing cyclinD1 (CCND1) and hyperphosphorylation of RB1, and via several pro-survival pathways, including NF-kappa-B, AKT1 and MAPK1/3(ERK1/2). Can also act as tumor suppressor upon mitogenicstimulation with PMA or TPA. In N-formyl-methionyl-leucyl-phenylalanine (fMLP)-treated cells, is required for NCF1 (p47-phox) phosphorylation and activation of NADPH oxidase activity,and regulates TNF-elicited superoxide anion production inneutrophils, by direct phosphorylation and activation of NCF1 orindirectly through MAPK1/3 (ERK1/2) signaling pathways. May alsoplay a role in the regulation of NADPH oxidase activity ineosinophil after stimulation with IL5, leukotriene B4 or PMA. Incollagen-induced platelet aggregation, acts a negative regulatorof filopodia formation and actin polymerization by interactingwith and negatively regulating VASP phosphorylation. Downstream ofPAR1, PAR4 and CD36/GP4 receptors, regulates differentiallyplatelet dense granule secretion; acts as a positive regulator inPAR-mediated granule secretion, whereas it negatively regulatesCD36/GP4-mediated granule release. Phosphorylates MUC1 in the C-terminal and regulates the interaction between MUC1 and beta-catenin. The catalytic subunit phosphorylates 14-3-3 proteins(YWHAB, YWHAZ and YWHAH) in a sphingosine-dependent fashion (Bysimilarity). Phosphorylates ELAVL1 in response to angiotensin-2treatment (PubMed:18285462). {ECO:0000250,ECO:0000269|PubMed:11748588, ECO:0000269|PubMed:11877440,ECO:0000269|PubMed:15774464, ECO:0000269|PubMed:16940418,ECO:0000269|PubMed:18285462, ECO:0000269|PubMed:19587372,ECO:0000269|PubMed:19801500}. |
| Retention analysis result of each fusion partner protein across 39 protein features of UniProt such as six molecule processing features, 13 region features, four site features, six amino acid modification features, two natural variation features, five experimental info features, and 3 secondary structure features. Here, because of limited space for viewing, we only show the protein feature retention information belong to the 13 regional features. All retention annotation result can be downloaded at . * Minus value of BPloci means that the break pointn is located before the CDS. |
| - In-frame and retained protein feature among the 13 regional features. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Protein feature | Protein feature note |
| - In-frame and not-retained protein feature among the 13 regional features. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Protein feature | Protein feature note |
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FusionGeneSequence for PRKCD_PRKCD |
| For in-frame fusion transcripts, we provide the fusion transcript sequences and fusion amino acid sequences. (nt: nucleotides, aa: amino acids) |
| * Fusion amino acid sequences. |
| * Fusion transcript sequences (only coding sequence (CDS) region). |
| * Fusion transcript sequences (Full-length transcript). |
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FusionGenePPI for PRKCD_PRKCD |
| Go to ChiPPI (Chimeric Protein-Protein interactions) to see the chimeric PPI interaction in . |
| Protein-protein interactors with each fusion partner protein in wild-type (BIOGRID-3.4.160) |
| Hgene | Hgene's interactors | Tgene | Tgene's interactors |
| - Retained PPIs in in-frame fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Still interaction with |
| - Lost PPIs in in-frame fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Interaction lost with |
| - Retained PPIs, but lost function due to frame-shift fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Interaction lost with |
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RelatedDrugs for PRKCD_PRKCD |
| Drugs targeting genes involved in this fusion gene. (DrugBank Version 5.1.0 2018-04-02) |
| Partner | Gene | UniProtAcc | DrugBank ID | Drug name | Drug activity | Drug type | Drug status |
| Hgene | PRKCD | Q05655 | DB05013 | Ingenol Mebutate | Protein kinase C delta type | small molecule | approved |
| Tgene | PRKCD | Q05655 | DB05013 | Ingenol Mebutate | Protein kinase C delta type | small molecule | approved |
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RelatedDiseases for PRKCD_PRKCD |
| Diseases associated with fusion partners. (DisGeNet 4.0) |
| Partner | Gene | Disease ID | Disease name | # pubmeds | Source |
| Hgene | PRKCD | C0011853 | Diabetes Mellitus, Experimental | 1 | CTD_human |
| Hgene | PRKCD | C0020538 | Hypertensive disease | 1 | CTD_human |
| Hgene | PRKCD | C0021841 | Intestinal Neoplasms | 1 | CTD_human |
| Hgene | PRKCD | C0023893 | Liver Cirrhosis, Experimental | 1 | CTD_human |
| Hgene | PRKCD | C0036572 | Seizures | 1 | CTD_human |
| Hgene | PRKCD | C0235032 | Neurotoxicity Syndromes | 1 | CTD_human |
| Hgene | PRKCD | C0242422 | Parkinsonian Disorders | 1 | CTD_human |
| Tgene | PRKCD | C0011853 | Diabetes Mellitus, Experimental | 1 | CTD_human |
| Tgene | PRKCD | C0020538 | Hypertensive disease | 1 | CTD_human |
| Tgene | PRKCD | C0021841 | Intestinal Neoplasms | 1 | CTD_human |
| Tgene | PRKCD | C0023893 | Liver Cirrhosis, Experimental | 1 | CTD_human |
| Tgene | PRKCD | C0036572 | Seizures | 1 | CTD_human |
| Tgene | PRKCD | C0235032 | Neurotoxicity Syndromes | 1 | CTD_human |
| Tgene | PRKCD | C0242422 | Parkinsonian Disorders | 1 | CTD_human |
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